AIR QUALITY CRITERIA
             FOR
             PHOTOCHEMICAL OXIDANTS
SUMMARY AND CONCLUSIONS
    U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE

                   Public Health Service
                  Environmental Health Service

-------
   3
                     AIR QUALITY CRITERIA
                                FOR
                  PHOTOCHEMICAL OXIDANTS
                    (The summary and conclusions herein
                     are reproduced from the original
                    volume as identified on this page.)


                              US EPA
                   Headquarters and Chemical Libraries
   ;                    EPA West Bldg Room 3340
 £                        Mailcode 3404T
 £p                    1301 Constitution Ave NW
 <£:                     Washington DC 20004
 o-                          202-566-0556
 /*

^    U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE

                            Public Health Service
                         Environmental Health Service
                    National Air Pollution Control Administration
                             Washington, D.C.
                              March 1970
                        Repository Material
                        !annanent Collection

-------
                                    Chapter  10.
                        SUMMARY AND CONCLUSIONS
A. INTRODUCTION
  This  document  is  a  consolidation and
assessment of the current state of knowledge
on the origin and effects of the group of air
pollutants known as photochemical oxidants
on  health,  vegetation,  and materials. The
purpose of this chapter is to provide a concise
picture of the information contained in this
document,  including conclusions  which are
believed reasonable to consider in evaluating
concentrations  of photochemical  oxidants
which are known to have an effect on either
health or welfare. Although nitrogen dioxide
is considered  one of the  photochemical
oxidants, it is  to  be subject  of  a  separate
report.  Consequently,  nitrogen  dioxide is
discussed in  this document only to the extent
that it participates in the formation and reac-
tions of other  photochemical  oxidants. The
information  and data contained in this docu-
ment  comprise the best available  bases,  and
provide  the  rationale  for development  of
specific  levels of standards of photochemical
oxidants in the ambient ah- for protection of
public health and man's environment.

B. NATURE OF PHOTOCHEMICAL
  OXIDANTS
  Photochemical oxidants result from a com-
plex series of atmospheric reactions initiated
by sunlight.  When reactive organic substances
and nitrogen oxides accumulate in the atmo-
sphere  and  are exposed  to  the  ultraviolet
component of sunlight, the formation of new
compounds, including ozone and peroxyacyl
nitrates, takes place.
  Absorption of ultraviolet light  energy by
nitrogen dioxide results in its dissociation into
nitric oxide and an  oxygen atom.  These
oxygen atoms for the most part react with air
oxygen to form ozone. A small portion of the
oxygen  atoms  and ozone react  also with
certain  hydrocarbons  to  form free  radical
intermediates and various products. In some
complex manner, the free radical  intermedi-
ates  and ozone  react  with the nitric oxide
produced initially. One  result of these reac-
tions is the very rapid oxidation of the nitric
oxide to nitrogen  dioxide and  an increased
concentration of ozone.
  The photochemical system  generally is ca-
pable of duplication in  the  laboratory. For
various  reasons,  however,  laboratory results
cannot be quantitatively extrapolated to the
atmosphere. Theoretically  generation  of an
atmospheric simulation model should be feasi-
ble,  enabling the prediction of ambient oxi-
dant  concentrations from a knowledge  of
emission and meteorological data.  The devel-
opment of such  a  model, however, is depen-
dent on the acquisition of more reliable and
applicable  quantitative  information derived
from direct atmospheric  observations, as well
as on the refinement of results obtained from.
irradiation chamber studies.

C. ATMOSPHERIC PHOTOCHEMICAL
  OXIDANT CONCENTRATIONS
  The presence  of photochemically  formed
oxidants has been indicated in all of the major
U.S. cities for which aerometric  data have
been  examined. On a  concentration basis,
ozone has been identified  as the major com-
ponent of the oxidant levels observed. Diffi-
culties arise, however,  in interpreting data
obtained by the most commonly used oxidant
measuring method; this method is nonspecific
and subject to several interferences. Adjusted
oxidant concentrations,  obtained  by correc-
ting  potassium iodide  oxidant measurements
                                         10-1

-------
for known interferences, have been found to
be  relatively close to  concurrent measure-
ments of ozone alone.
   Since photochemical  oxidants are the pro-
ducts of atmospheric  chemical reactions, the
relationship between precursor emissions and
atmospheric oxidant concentrations is  much
less  direct  than is  the  case  for  primary
pollutants. A further complicating situation is
the dependence of these photochemical reac-
tions on intensity and  duration of sunlight,
and on temperature.
   In an analysis of  oxidant  concentration
data for 4 years and 12  stations, the  daily
maximum  1-hour average  concentration was
equal to or exceeded  290 jug/m3 (0.15  ppm)
up  to   41  percent  of  the time; maximum
1-hour  average  concentrations  ranged  from
250  to 1,140 jug/™3 (0.13 to  0.58 ppm);
short-term peaks were as high as 1,310 jug/™3
(0.67 ppm). Yearly averages, commonly app-
lied to other pollutants,  are not representative
of air quality with  respect to oxidant pollu-
tion, because 1-hour average ozone concentra-
tions will necessarily be at or about zero for
approximately 75 percent of the time  when
photochemical reactions are minimal.
   Peroxyacyl nitrates, through not routinely
measured, have been identified  in the atmo-
sphere   of several cities.  These compounds
may be assumed to be present  whenever
oxidant levels are elevated.
D. NATURAL SOURCES OF OZONE
   Ozone  can be  formed  naturally in  the
atmosphere by electrical discharge, and in the
stratosphere by  solar  radiation, by processes
which   are not capable of producing signifi-
cant urban concentrations of this pollutant.
Maximum instantaneous ozone levels of from
20 to  100 /ig/m3 (0.01 to  0.05 ppm) have
been recorded in nonurban areas.
E. MEASUREMENT OF PHOTOCHEMICAL
   OXIDANTS
   The  most widely used technique  for the
analysis of atmospheric total oxidants is based
on the reaction of these compounds  with
potassium iodide to release iodine. The iodine
may then be measured by either colorimetnc
or coulometric methods. Calibrating the oxi-
dant measurement  method used  against a
known quantity of ozone provides a measure-
ment of the  net oxidizing  properties  of the
atmosphere in terms of an equivalent concen-
tration of ozone. Most oxidant measurements
are currently  being made by the colorimetric
method, although coulometric analyzers are
used in a number of laboratory and field studies.
   In order to generate comparable data, it is
essential that all measurements be made by
techniques which have been calibrated against
the same standard or reference method. Since
at  the  present time there is no standard
method for the  determination of total oxi-
dants,  the  National Air  Pollution Control
Administration  recommends use of the neu-
tral-buffered  1 percent potassium iodide col-
orimetric technique  as  the method  against
which  all  instruments  and other methods
should be compared. In addition to serving as
a manual procedure for determining oxidants,
the reference  method may be used  in conjunc-
tion with a "dynamic calibration" technique
for instrumental methods.
   Reducing  agents  such as sulfur dioxide
produce a  negative interference  in oxidant
determination. Such interference  can  be re-
duced, however, by passing the  air stream
through a chromium trioxide  scrubber prior
to measurement. Unfortunately, a portion of
the nitric oxide which may be present in the
air stream is oxidized to nitrogen  dioxide by
the  scrubber. This results  in an apparent
increase in the oxidant measurement of about
11  percent  of the concentration of  nitric
oxide.  Moreover, a portion of the  atmospher-
ic nitrogen dioxide  concentration will also
contribute to the oxidant measurement. Per-
oxyacyl nitrate  concentrations  are  usually
small  and  contribute   only  a  very   slight
amount to the oxidant reading.
   There  are  several means for the specific
measurement  of atmospheric  ozone. Instru-
mental  methods  include  chemiluminescent
analysis based on the reaction of ozone with
Rhodamine B, gas phase olefin titration, and
10-2

-------
ultraviolet and infrared spectroscopy. A semi-
quantitative method for  ozone measurement
is based on its  ability to produce cracks in
stretched rubber. Peroxyacyl nitrates can be
measured in the atmosphere by gas chromato-
graphy  with  the use of an electron-capture
detector.
   For a better  evaluation of  the results of
research on  the  effects of  photochemical
oxidants, it is essential that  data be obtained
for individual oxidants such as  nitrogen diox-
ide, ozone, PAN, formaldehyde, acrolein, and
organic peroxides.  These data would  either
replace or complement data on total oxidants.
Instrumentation   currently  available permits
the  accurate  measurement of atmospheric
ozone,  nitrogen  dioxide, and PAN.  There
exists, however,  a  further  need  to develop
instruments capable of measuring other indi-
vidual gaseous  pollutants   which have  the
properties of  oxidants. Photochemical reac-
tions  and problems derived from oxidants can
be much better  defined using specific  meth-
ods for measurement  in preference  to  the
traditional total oxidants determination.

F. EFFECTS OF PHOTOCHEMICAL
   OXIDANTS ON  VEGETATION
   AND MICROORGANISMS
   Injury to vegetation is one of the earliest
manifestations  of  photochemical air  pollu-
tion,  and sensitive plants are useful biological
indicators  of this type of pollution.  The
visible symptoms of photochemical oxidant
produced  injury to plants may be classified
as: (1) acute injury, identified by cell collapse
with  subsequent development of  necrotic
patterns;  (2)  chronic injury,  identified by
necrotic patterns with or without chlorotic or
other pigmented patterns; and, (3) phsyiologi-
cal effects, identified by growth alterations,
reduced yields, and changes in  the quality of
plant  products.  The  acute  symptoms are
generally characteristic of a specific pollutant;
though highly characteristic,  chronic  injury
patterns are  not. Ozone injury to leaves  is
identified  as  a  stippling or  flecking. Such
injury has occurred experimentally  in the
most sensitive  species after  exposure to 60
jug/m3 (0.03 ppm) ozone for 8 hours. Injury
will  occur in shorter time periods when low
levels of sulfur dioxide are present. PAN-pro-
duced injury is characterized by an under-sur-
face glazing or bronzing  of the  leaf. Such
injury has  occurred experimentally in the
most sensitive  species after  exposure  to 50
jug/m3 (0.01 ppm)  PAN for 5 hours. Leaf
injury has occurred in certain sensitive species
after a 4-hour  exposure  to 100 jig/m3 (0.05
ppm) total oxidant. Ozone appears to be the
most important phytotoxicant in the photo-
chemical complex.
  There  are a number of factors affecting the
response  of vegetation to photochemical air
pollutants. Variability in response is known to
exist between  species  of a given  genus and
between  varieties within a given species; varie-
tal  variations  have been  most  extensively
studied with tobacco. The influence of light
intensity on the sensitivity of plants to damage
during growth appears to depend on the phy-
totoxicant. Plants  are more sensitive to PAN
when grown under high  light intensities, but
are more sensitive to ozone when grown under
low  light intensities. Reported findings are in
general agreement  that sensitivity of  green-
house-grown plants to oxidants increases with
temperature, from  10° to 38° C (40° to 100°
F), but this  positive correlation  may result
from the overriding influence of light intensi-
ty on sensitivity. The effects of humidity on
the  sensitivity  of  plants has not  been  well
documented. General  trends indicate  that
plants  grown  and/or exposed  under high
humidities  are  more  sensitive than  those
grown at low humidities.  There has been little
research   in  this  direction,  but  there  are
indications  that soil factors  such as drought
and  total fertility  influence the sensitivity of
plants to  phytotoxic air pollutants. The age of
the leaf  under  exposure  is important in de-
termining its  sensitivity  to  air  pollutants.
There is some evidence that oxidant or ozone
injury may be reduced by pretreatment with
the toxicant.
                                                                                     10-3

-------
   Identification of injury to a plant as being
caused by air pollution is a difficult undertak-
ing. Even when the markings on the leaves of
a plant may be identified with an air pollut-
ant, there is the further  difficulty of evaluat-
ing the injury in terms of its effect  on the
intact plant. Additional problems  arise in
trying to evaluate the economic impact of
air pollution damage to a plant.
   The  interrelations  of time  and  concen-
tration (dose) as they affect injury to plants
are essential to air quality criteria. There  are,
however,  only  scant  data relating concen-
trations  and  length  of  photochemical oxi-
dant  exposure to chronic injury and  effects
on reduction  of plant  growth,  yield,  or
quality.  There  is also  a  dearth  of  infor-
mation   relating  concentrations  to   acute
injury. A larger body of information exists
on the  acute effects of ozone,  but  even in
this instance,  the  information is far from
complete. Sufficient data do exist, however,
to  tabularly  present  ozone  concentrations
which will produce 5 percent injury to sensi-
tive, intermediate, and resistant plants after
a  given  short-term  exposure, as shown in
Table  10-1. Information available  lists 20
species  and/or varieties  as sensitive,  55  as
intermediate in sensitivity, and 64 as rela-
tively resistant.
   Bacteriostatic and bacteriocidal properties
of  photochemical oxidants in  general have
been  demonstrated.  The growth suppression
of microorganisms by  ozone is a well-known
phenomenon, although  the  ozone  concen-
trations for  this activity are undesirable from
a  human   standpoint.  The  bacteriocidal
activity  of ozone  varies  with its  concen-
tration,  the  relative  humidity,   and  the
species of bacteria.

G. EFFECT OF OZONE ON MATERIALS
  The detailed, quantitative extent of damage
to materials caused by atmospheric  levels of
ozone is unknown,  but generally any organic
material is  adversely affected by concentrated
ozone. Many polymers are extremely sensitive
to even very small  concentrations of ozone,
this sensitivity increasing with the number of
double bonds in the structure of the polymer.
  Economically, rubber is probably the most
important  material  sensitive to ozone attack,
particularly styrene-butadiene, natural, poly-
butadiene,  and synthetic polyisoprene.  Anti-
ozonant  additives have  been  developed and
are  capable  of protecting elastomers from
ozone degradation; synthetic  rubbers with
inherent  resistance to  ozone are also available.
These additives  are expensive, however, and
add  to  the  cost   of the  end product; in
addition, increasing amounts of antiozonants
are required as the  amount of ozone which is
to be encountered  increases,  and  sometimes
only temporary protection is provided.
  Ozone   attacks   the  cellulose  in  fabrics
through both a  free radical chain mechanism
and  an electrophilic attack on double bonds;
light  and humidity appear necessary for ap-
preciable alterations  to  occur. The relative
susceptibility  of different  fibers to  ozone
attack appears  to  be,  in  increasing  order,
cotton, acetate, nylon, and polyester.
              Table 10-1. PROJECTED OZONE CONCENTRATIONS WHICH WILL PRODUCE, FOR
                  SHORT-TERM EXPOSURES, 5 PERCENT INJURY TO ECONOMICALLY
                  IMPORTANT VEGETATION GROWN UNDER SENSITIVE CONDITIONS

Time,
hi
0.2
0.5
1.0
2.0
4.0
8.0
Ozone concentrations producing injury in three types of plants, ppm
Sensitive
0.35-0.75
0.15-0.30
0.10-0.25
0.07-0.20
0.05-0.15
0.03-0.10
Intermediate
0.70-1.00
0.25-0.60
0.20-0.40
0.15-0.30
0.10-0.25
0.08-0.20
Resistant
0.90 and up
0.50 and up
0.35 and up
0.25 and up
0.20 and up
0.15 and up
10-4

-------
  Certain dyes are susceptible to fading during
exposure to ozone. The rate and extent of fad-
ing is also dependent upon other environmental
factors  such  as  relative  humidity and  the
presence of air pollutants other than ozone, as
well as the length and concentration of ozone
exposure and the type of material exposed.
H. TOXICOLOGICAL STUDIES OF
   PHOTOCHEMICAL OXIDANTS
1. Effects of Ozone in Animals
  The major  physiological effects of ozone
are on the respiratory system. Inhalation of
ozone  at  concentrations greater than about
5,900 pg/m3 (3 ppm) for several hours pro-
duces hemorrhage and  edema in  the lungs.
This reaction can be fatal to animals. Rats and
mice appear to be more sensitive than rabbits,
cats, and guinea pigs. The toxicity is greater
for young animals and for exercising animals.
It is abated by intermittency  of exposure, by
prophylactic  administration  of  chemical re-
ducing agents, or by introducing agents into
the diet which  reduce  the  activity  of  the
thyroid  gland. At exposures  less than those
which produce edema in the lungs, changes in
the mechanical properties of  the lung occur.
These are accompanied by increased breathing
rates and increased oxygen consumption.  Re-
peated non-fatal exposures to concentrations
greater than  15,700 jug/m3 (8 ppm) for 30
minutes have produced fibrosis in the respira-
tory tract  of rabbits, with the  damage increas-
ing  in severity over the length of the respira-
tory tract from the trachea to the bronchioles.
  Short-term  exposures  to ozone  also pro-
duce chemical changes in the lung  tissue ele-
ments of  animals. A  study conducted on a
small number  of rabbits  showed that inhala-
tion  of  1,960  to  9,800  Mg/m3 (1 to  5 ppm)
ozone for  1 hour can produce  denaturation of
the structural  lung  proteins.  Ozone also  ap-
pears to  oxidize the sulfhydryl  groups of
amino acids in the lung.
  Short-term  exposures  to ozone  also pro-
duce changes in organs other than the lung.
Concentrations of 5,900 jug/m3 (3 ppm) for
20 hours  can  stimulate some adaptive liver
enzymes.  Inhalation of  390  to 490
 (0.2 to 0.25 ppm) ozone for 30 to 60 minutes
 makes the red  blood cells of mice, rabbits,
 rats, and man more sensitive to the shape-al-
 tering effects  of' irradiation. Exposure of
 blood to ozone  in vitro produces interference
 with  the release of oxygen from red blood
 cells; this suggests that ozone exposure could
 impair the delivery of oxygen to the tissues.
 Ozone   exposures  at  concentrations  from
 1,310 to 7,800 jug/m3 (0.67 to 4.0 ppm) have
 been  shown to reduce the in vitro phagocytic
 abilities of the pulmonary alveolar macrophag-
 es. A 3-hour exposure  to 9,800 jug/m3 (5
 ppm)  ozone has been shown to reduce the
 activity  of bactericidal enzyme, presumably
 due to in vivo oxidation of the enzyme.
   Ozone inhalation increases the vulnerability
 of animals to other agents.  A single exposure
 to  ozone at  a  concentration  of  160 jug/m3
 (0.08  ppm)  for  3 hours  has increased the
 mortality among  mice from inhalation of
 pathogenic bacteria. This occurred when the
 bacteria  were administered both before  and
 after exposure to ozone. Ozone also increases
 the toxicity of histamine in  guinea pigs.
  Long-term effects  of ozone exposure in-
clude,  in some species, the development of
tolerance to  biological  effects  of ozone,
production of fibrotic changes in the lungs,
and a possible increase in the rate of aging.
While tolerance has been shown in rodents, it
has not been shown in chickens, and it is not
certain whether  or  not it occurs in man. In
species where tolerance to ozone exposure has
been demonstrated, information is not avail-
able concerning the duration and mechanism
of tolerance following repeated exposure. The
aging  effect  may be  similar to the changes
produced by exposure to free radicals or by
irradiation.

2. Effects of Ozone in Humans
  Some studies of human exposures to ozone
have focused on the determination of  the
threshold level at*which odor can be detected,
and on the occurrence of changes in pulmo-
nary function. Nine out of 10 subjects ex-
posed to 40 pig/m3 (0.02 ppm)  ozone were
able to detect the odor immediately, and it
                                                                                   10-5

-------
 persisted for an average of 5 minutes. Thir-
 teen of 14  subjects  exposed to 100  pg/m3
 (0.05 ppm)  ozone  indicated  the  odor  is
 considerably  stronger at  this concentration,
 and the odor persisted for an average of 13
 minutes.
   Occupational exposure of humans to ozone
 concentrations of up to 490 jug/m3  (0.25
 ppm) has not produced detectable changes in
 pulmonary  function.  Respiratory  symptoms
 and a decrease in vital capacity in three  out of
 seven smokers who had been  occupationally
 exposed  to ozone have occurred at concentra-
 tions greater than 590 jug/m3 (0.3 ppm).
   Experimental  exposures of  humans have
 been carried  out at  concentrations ranging
 from 200  to 7,800 /ug/m3  (0.1  to about  4
 ppm) for periods of up to 2 hours. Exposure
 to 390 ng/m3 (0.2 ppm) for 3 hours daily,  6
 days a week, for 12 weeks has not produced
 any  change  in  ventilatory  function  tests.
 Similar  exposure to  980 jug/m3 (0.5  ppm)
 produced a decrease in the forced expiratory
 volume  during the last 4 weeks of exposure,
 with recovery  taking  place in  a subsequent
 6-week period. In each of  11 subjects, expo-
 sure  to  1,180 to 1,570 jug/m3  (0.6  to 0.8
 ppm) for 2 hours resulted in an impairment of
 the  diffusing capacity of the  lung.  Small
 decreases in vital capacity and forced expira-
 tory volume were observed in some of these
 subjects.  Resistance to flow  of air  in  the
 respiratory tract increased slightly in some sub-
jects after  exposure to 200 to  1,180  /ug/m3
 (0.1  to 0.6 ppm) for 1  hour, and increased con-
 sistently in each of four subjects after exposure
 to 1,960  Mg/m3 (1 ppm) for 1 hour.
  Data  obtained from animal experimenta-
tion cannot  be used  directly  to define  the
ozone concentrations  above which  human
health will  be  affected.  Animal  mortality
studies, however, can be useful in determining
the  factors  involved  in  toxicity. While  the
concentrations of ozone used in the  deter-
mination of short-term non-fatal  effects in
animals are rarely found in ambient air, the
changes in pulmonary function observed dur-
ing and after exposure to these concentrations
 call attention to the possibility  that similar
 effects may be observed in humans.
   When interpreting the research conducted
 thus  far  using  human  subjects,  it must be
 noted that occupational exposures differ from
 experimental exposures, because it is difficult
 in an occupational environment to define the
 exact  nature and  dose  of  the pullutants
 present.
 3. Effects of Peroxyacetyl Nitrate
   Experimental  studies  with peroxyacetyl ni-
 trate (PAN) in animals indicate that mortality
 may  be  delayed  for 7  to   14  days  after
 exposure; however, the exposure levels requir-
 ed  to produce  this mortality  never occur in
 ambient atmospheres.
  A  single experimental study  of healthy
 human subjects exposed to 1,485 jug/m3 (0.3
 ppm) peroxyacetyl nitrate indicated only that
 there may  be   a  small increase  in oxygen
 uptake  with exercise.  Sensitive  pulmonary
 function tests were not obtained.
  The data from animal and  human studies
 are sparse and inadequate for determining the
 toxicological potential  of peroxyacetyl ni-
 trate. It would appear,  however,  that at the
 concentrations of  this compound known to
 occur in ambient atmospheres, PAN does not
 present any recognized health hazard.

4. Effects of Mixtures Containing Photo-
chemical Oxidants on Animals

  Studies have  been conducted  on animals
 exposed to both synthetic and natural photo-
 chemical  smog.  Synthetic smog has  been
 produced by the irradiation of diluted motor
 vehicle exhaust or by irradiation  of air mix-
 tures  containing nitrogen oxides and certain
 hydrocarbons. Exposures to irradiated motor
 vehicle exhaust are complicated by the simul-
 taneous presence of  carbon  monoxide and
 other non-oxidant substances  which include
 high concentrations of formaldehyde. Guinea
 pigs show increased respiratory volume during
a four-hour exposure to irradiated exhaust
 containing   1,570  /ig/m3  (0.8  ppm)  total
oxidant.
10-6

-------
  Exposure of  mice  to  both  natural and
synthetic smog for 3 hours, at concentrations
greater than 780 Mg/m3 (0.4 ppm) oxidants
have produced changes in the fine structure of
the  lung.  The  nature  and  extent of  the
damage was the same after exposure to either
type of smog with the same oxidant levels.
The severity of the damage increased with age
and became irreversible at age 21 months.
  Chronic exposure of guinea pigs to ambient
air with an average oxidant concentration of
from 40  to 140 Mg/m3 (0.02  to 0.07  ppm)
leads to a  significant increase  in flow resist-
ance when the peak  oxidant concentrations
exceed 980 Mg/m3 (0-5 ppm).
  When male  mice,  prior to mating, were
given long-term exposures to  irradiated auto
exhaust containing from 200 to 1,960 /-tg/m3
(0.1  to 1.0  ppm)  oxidant,  a  decrease  in
fertility and an increase in neonatal mortality
of their  offspring resulted;  the  irradiated
mixture also contained varying concentrations
of carbon  monoxide, nitrogen  oxides, and
hydrocarbons.  Similar exposures also cause a
reduction  in   spontaneous running activity,
which results in an adaptation response.
  Thus a  number of experimental studies
have demonstrated that changes in lung tissue
or lung  function occur  when  animals  are
exposed for several hours to  photo-oxidized
mixtures containing 980 Mg/m3 (0.5 ppm) or
more of oxidants.

5. Effects of Mixtures Containing Photo-
chemical Oxidants on Humans
  Laboratory  studies of human exposure to
photochemical smog have involved  primarily
the measurement of eye irritation.  Based on
the  existing data,  it appears that:  (1)  the
effective eye  irritants are the  products  of
photochemical reactions;  (2)  although oxi-
dant concentrations may  correlate  with  the
severity of eye irritation, a direct cause-effect
relationship has not been demonstrated since
ozone, the principal contributor to ambient
oxidant levels  is not an eye irritant; (3)  the
precursors  of  the eye  irritants are organic
compounds in combination with oxides of
nitrogen,  the  most potent being  aromatic
hydrocarbons; (4) the chemical identities of
the effective irritants in synthetic systems are
known as being formaldehyde, peroxybenzoyl
nitrate (PBzN),  peroxyacetyl nitrate (PAN),
and  acrolein, although the latter two contri-
bute  to  only a  minor extent;  and (5)  the
substances causing eye irritation  in the atmo-
sphere have not been competely defined.

I. EPIDEMIOLOGICAL STUDIES OF PHO-
   TOCHEMICAL OXIDANTS
   Several studies have examined daily mortal-
ity rates  in localities where photochemical air
pollution occurs, to determine if a relation-
ship exists with  increased levels of oxidant.
Such an association  has  not  been shown.
These  studies,  however,  pose  a number  of
unresolved questions. One of these is, what is
the effect of temperature, either alone or in
combination with oxidants?  In  some of the
most severe episodes, there has  been an
associated increase in environmental tempera-
ture, sufficient  to cause excess mortality by
itself. Several studies of mortality among resi-
dents in nursing homes in Los Angeles showed
such  excess mortality. In recent heat wave
and  air  pollution  episodes, however, large
proportions  of  the  elderly and ill persons in
nursing homes  have  been protected  by air
conditioning.
   Evidence  of increased morbidity  has been
sought  through  study of  general hospital
admissions,  but  no unequivocal association
between  photochemical air pollution and in-
creased morbidity has been shown. Additional
studies are indicated for improved definition.
Peak  oxidant  values  of  250 //g/m3 (0.13
ppm), which might be expected in relation to
maximum hourly average levels of 100 to 120
/jg/m3 (0.05 to  0.06 ppm), have been associa-
ted with aggravation of asthma. No associa-
tion  between ambient oxidant concentrations
and changes  in respiratory  symptoms or func-
tion  was shown, however,  in  two separate
studies of subjects  with preexisting chronic
respiratory   disease.  Non-smoking  subjects
with chronic respiratory disease did, however,
demonstrate less airway resistance when they
were studied in a room where the ambient air

                                      10-7

-------
of Los Angeles was filtered before entry. No
acute or chronic effects of oxidant pollution
on  ventilatory  performance of elementary
schoolchildren were demonstrated in a study
conducted in two communities within the Los
Angeles basin.
  Impairment of performance by high school
athletes has been observed when photochemi-
cal oxidants  ranged from 60 to 590 /ug/m3
(0.03 to  0.3 ppm) for 1  hour immediately
prior  to the  start of activities.  Significantly,
more automobile accidents have also occurred
on days of high oxidant concentrations, but
no threshold  level  for  this effect could be
determined from the analysis.
  Among the general community, eye irrita-
tion  is a major effect of photochemical air
pollution. In Southern  California, it has af-
fected more than three-fourths of the popula-
tion. Eye irritation under conditions prevalent
in Los Angeles  is likely to occur in a large
fraction  of  the  population when  oxidant
concentrations  in ambient  air  increases to
about 200 jug/m3 (0.10 ppm).  This oxidant
value might be expected to be associated with
a maximum  hourly average oxidant concen-
tration of 50 to 100 Mg/m3 (0.025 to 0.50
ppm), depending on  localized  conditions.
According to survey data gathered in  1956,
asthma, cough,  and nose  and throat  com-
plaints were  more frequent  in Los Angeles,
Orange, and  San  Diego counties than in the
San Francisco Bay area or in the rest of the
State.
  Casual  reports  of  the  presence of the
symptoms of eye irritation have been record-
ed in many cities  in the United  States.
Epidemiologic studies have been inadequate,
however, to relate these symptoms clearly to
measured  exposures to photochemical oxi-
dants. In fact, one of the major photochemi-
cal  oxidants, ozone, is not  an  eye irritant.
That  eye irritation  is experienced whenever
the oxidant level  exceeds a certain value is an
indication that oxidant concentrations corre-
late  well with other  aspects of the  photo-
chemical complex; oxidant levels are probably
a measure  of the  photochemical  activity
which produces the eye irritants. On the other
hand, it must be recognized that reactions of
ozone  with  hydrocarbons do lead to hydro-
carbon fragments which are eye irritants. Nor
can the possibility be discounted that ozone
in the photochemical complex may  exert a
synergistic effect on eye irritation.  Because
the oxidant reading measured  only  the  net
oxidizing property  of the  atmosphere, how-
ever,  the same  amount  of  eye irritation
experienced  in  two  different geographical
locations from  identical irritants could  be
associated with different levels of oxidant, if
other pollutants differed in their concentra-
tion.
J. AREAS FOR FUTURE RESEARCH
1. Environmental Aspects of Photochemical
Oxidants
  1. Research should be conducted to further
    identify the substance(s)  which cause
    eye irritation.
  2. The nature of the  photochemical aero-
    sol, its behavior at different pressures of
    water  vapor,  and   the  nature  of  the
    surface  layer of the particulates  remains
    to be determined.
  3. The role of sulfur dioxide in the forma-
    tion of photochemical aerosols  and in
    the  impairment of  visibility should  be
    investigated.
  4. Mechanisms  of photochemical  oxidant
    formation should be explained.
2. Toxicity of Ozone, Photochemical
Oxidants, and Peroxyacyl Nitrates
   l.The  effect  of  ozone  and PAN   in
    combination with other pollutants found
    in  ambient air should be investigated.
    Considerable information is available on
    the  separate effects of ozone, nitrogen
    dioxide, and sulfur dioxide, but  data  on
    the combined effects of defined  concen-
    trations of these gases are sparse. The
    effect of particulates (dust, saline drop-
    lets, oil, soots, etc.)  should be deter-
    mined  alone and  in combination with
    the  gases.  Additional  variables  such as
10-8

-------
     humidity  and  temperature should  be
     controlled and  recorded. These  experi-
     ments should be carried out with materi-
     als, vegetation,  animals, and, under ap-
     propriate conditions, in man.
  2. Experiments with human exposures  to
     gas  mixtures should include a  compari-
     son  between  the  respiratory  effects
     shown  in healthy  subjects and those
     shown  in patients with chronic respira-
     tory disease, care being taken to  respect
     the rights of experimental subjects.
  3. Existing data demonstrate that  tolerance
     occurs  only in  rodents.  Indices other
     than mortality  are required to demon-
     strate tolerance  in animals.  If such in-
     dices can be developed, then a study is
     needed to see if a similar phenomenon
     occurs in man.
  4. The mechanisms of systemic effects  of
     ozone (headache, fatigue, impaired oxy-
     gen transport by hemoglobin,  inability
     to  concentrate,  etc.) have  yet to be
     explained.
  5. The rate and site of uptake of ozone and
     its fate following uptake should be deter-
     mined in vegetation and animals.
  6. The  mechanism for the production  of
     ozone-induced   pulmonary   edema  re-
     mains unexplained.
  7. Additional research  in needed  to define
     the  role of peroxyacyl nitrates  in the
     production of eye irritation.
3. Epidemiology of Photochemical Oxidants
  1. Of high priority is the need  to study eye
     and respiratory irritation in metropolitan
     areas  outside   of  California.  Studies
     should  be supplemented by pulmonary
     function tests.
  2. Although the effects of episodes  of high
     pollution levels  have been studied with
     respect to mortality, morbidity, impair-
     ment  of performance, etc., additional
     studies are needed at different  sites and
     for  different  effects.  These should in-
     clude   congenital malformations,  still-
     births,  hospitals admissions  for miscar-
     riage, and alterations in the sex ratio of
     newborns.
   3. The examination of children has received
     insufficient  attention in  epidemiologic
     studies  of  the  health  effects  of  air
     pollution. This  should  be undertaken
     with respect to the  effects of photo-
     chemical oxidants  using simple pulmon-
     ary function tests. Emphasis should be
     placed  on  further studies of the inci-
     dence of asthma attacks during episodes
     of high pollution.

K.  CONCLUSIONS
   Derived from a careful  evaluation of the
studies  cited in this  document,  the conclu-
sions given below represent the best judgment
of  the  scientific staff  of  the  National Air
Pollution  Control Administration of  the  ef-
fects  that may occur when various levels of
photochemical  oxidants are  reached in the
ambient air.  The more detailed information
from which the conclusions were derived, and
the qualifications that entered-  into the con-
sideration of these data, can be found in the
appropriate chapter of this document.

1. Human Exposure
a.  Ozone

(1) Long-term exposure of
    human subjects.
    (a)  Exposure to a concentration of up to
        390  /ig/m3 (0.2 ppm) for 3 hours a
        day, 6 days a week, for  12 weeks, has
        not  produced  any apparent  effects
        (Chapter 8, section B.2.)
    (b)  Exposure to a concentration of 980
       /Ltg/m3  (0.5 ppm) for  3  hours a day,
       6 days a week, has caused a decrease
       in the  1-second  forced expiratory
       volume   (FEVli0)  after  8  weeks
       (Chapter 8, section B.2)
(2) Short-term exposure of
    human subjects.
    (a)  Exposure to  a  concentration of  40
        Mg/m3   (0.02  ppm)   was detected
        immediately  by 9  of  10 subjects.
                                                                                    10-9

-------
        After  an  average of 5 minutes expo-
        sure, subjects could no longer detect
        ozone (Chapter 8, section E.2).
     (b) Exposure to a  concentration of 590
        jug/m3 (0.3 ppm) for 8 hours appears
        to be the threshold for nasal and throat
        irritation (Chapter 8, section E.2.)
    (c) Exposure to concentrations of from
        1,180 to  1,960 jug/m3  (0.6 to 1.0
        ppm) for 1  to 2 hours may impair
        pulmonary  function by  causing in-
        creased  airway resistance, decreased
        carbon monoxide diffusing capacity,
        decreased  total capacity,  and  de-
        creased   forced  expiratory   volume
        (Chapter 8, section  B.2'.)
    (d) Exposure to concentrations of from
        1,960 to 5,900 Mg/m3  (1.0 to 3.0
        ppm) for 10  to 30 minutes is in-
        tolerable to  some people  (Chapter 5,
        section B.2.)
    (e) Exposure   to   a  concentration  of
        17,600  Mg/m3  (9.0  ppm)  produces
        severe illness (Chapter 5, section B.2.)
b. Oxidants

(1) Long-term exposure of human
    subjects.
   Exposure  to  ambient air  containing an
   oxidant   concentration  of  about  250
   /ig/m3  (0.13  ppm)  (maximum  daily
   value) has caused  an  increase  in the
   number  of asthmatic attacks in about 5
   percent of a group of asthmatic patients.
   Such a peak value would be expected to be
   associated with a maximum hourly average
   concentration of  100 to 120jug/m3 (0.05
   to 0.06 ppm) (Chapter 9, section B.3.)

(2) Short-term exposure of
    human subjects.
    (a) Exposure to an atmosphere with peak
        oxidant concentrations of 200 /ig/m3
        (0.1   ppm) and  above has been  asso-
        ciated with eye irritation. Such a peak
        concentration would be expected  to
        be associated with a maximum hourly
        average concentration of 50  to 100
       /zg/m3 (0.025 to 0.05 ppm) (Chapter 9,
       section B.3.)
    (b) Exposure to an atmosphere with aver-
       age  hourly  oxidant  concentrations
       ranging from 60 to 590 Mg/m3 (0.03 to
       0.30 ppm) has been associated with
       impairment of performance  of stu-
       dent athletes (Chapter 9, section B.4.)
2. Other Exposures
a. Photochemical Oxidants
(1) Effects on vegetation and
    laboratory animals.
    (a) Exposure  to  concentrations of about
       60 Mg/m3  (0.03 ppm) ozone for 8
       hours or  to  0.01  ppm  peroxyacetyl
       nitrate for 5 hours has been associa-
       ted with the  occurence of leaf lesions
       in the most  sensitive species, under
       laboratory  conditions (Chapter 6, sec-
       tion E.)
    (b) Exposure  to ambient air containing
       oxidant concentrations  of about 100
       Mg/m3  (0.05  ppm) for 4  hours  has
       been associated with leaf injury to the
       most sensitive  species  (Chapter  6,
       section E.)
    (c) Experimental exposures of laboratory
       animals to ozone concentrations  of
       from  160  to 2,550 MS/m3  (0.08  to
       1.30 ppm) for 3 hours has resulted in
       increased  susceptibility  to  bacterial
       infection (Chapter 8, section B.I.)
b. Ozone Effects on Susceptible Materials
(1) Polymers.
    (a) Many polymers, especially rubber, are
       extremely  sensitive to very small con-
       centrations.  To  provide protection,
       antiozonant additives are used, but are
       expensive and add to  the cost of the
       end product (Chapter 7).
(2) Cellulose and dyes.
    (a) The cellulose in fabrics is attacked by
       ozone, with subsequent weakening of
       the fabric. Similarly, certain dyes are
       susceptible to fading during exposure
       to ozone   (Chapter 7). Tables 10-2
 10-10

-------
                                                    Table 10-2. EFFECTS OF OZONE
Effect
Vegetation damage2
Cracking of stretched rubber

Odoi detection
Increased susceptibility of
laboratory animals to
bacterial infection
Respiratory irritation (nose
and throat), chest constriction
Changes in pulmonary function:
Diminished FEVj Q after
8 weeks

Small decrements in VC, FRC,
and DL^jQ in, respectively ,3,
2, and 1 out of 7 subjects
Impaired diffusion
capacity (DL^Q)

Increased airway resistance


Reduced VC, severe cough,
inability to concentrate
Acute pulmonary edema


Exposure
ppm
0.03
0.02

0.02
0.08
to
1.30
0.30


0.50


0.20
to
0.30
0.60
to
0.80
0.10
to
1.00
2.00

9.00


ttgjm3
60
40

40
160
to
2,550
590


980


390
to
590
1,180
to
1,570
200
to
1,960
3,900

17,600


Duration
8 hours
1 hour

<5 minutes
3 hours


Continuous during
working hours

3 hours/day,
6 days/week, for
12 weeks
Continuous during
working hours

2 hours


1 hour


2 hours

Unknown


Comment
Sensitive species; laboratory conditions
Vulcanized natural rubber

Odor detected in 9 of 10 subjects
Demonstrated in mice at 160 fig/m
and in mice at 2550 Mg/m3

Occupational exposure of welders,
other pollutants probably also present
Experimental exposure of 6 subjects.
Change returns to normal 6 weeks after
exposure. No changes observed at 390^g/m3
(0.2 ppm)
Occupational exposure. All 7 subjects
smoked. Normal values for VC, FRC, and
DLCO based on predicted value.
Experimental exposure of 11 subjects


Significant increase in 2 of 4 subjects
at 200 Mg/m3 (0.1 ppm) and 4 of 4 subjects
at 1960Mg/m3(1.0ppm)
High temperatures. One subject.

Refers to peak concentration of occupa-
tional exposure. Most of exposure was
to lower level
Reference
Heck and Dunning
Bradley and
Haagen-Smit
Henschler et al.
Coffin et al.
Miller et al.

Kleinfeld et al.

Bennett



Young et al.


Young et al.


Goldsmith et al.


Griswold et al.

Kleinfeld et al.


Similar vegetation damage also occurs upon exposure to 0.01 ppm peroxyacetyl nitrate for 5 hours.

-------
o
to
                               Table 10-3. EFFECTS ASSOCIATED WITH OXIDANT CONCENTRATIONS IN PHOTOCHEMICAL SMOG
Effect
Vegetation damage

Eye irritation



Aggravation of respiratory
diseases- asthma





Impaired performance of stu-
dent athletes

Exposure,
ppm
0.05

Mg/m3
100

Exceeding
0.1


0.13a






0.03
to
0.30
200


250






60
to
590
Duration
4 hours

Peak values



Maximum daily
value





1 hour


Comment
Leaf injury to sensitive species
Result of panel response.
Such a peak value would be expected
to be associated with a maximum
hourly average concentration of
50 to 100 Mg/m3 (0.025 to 0.05 ppm)
Patients exposed to ambient air. Value
refers to oxidant level at which number
of attacks increased
Such a peak value would be expected to
be associated with a maximum hourly
average concentration of 100 to 120
Mg/m (0.05 to 0.06 ppm).
Exposure for 1 hour immediately prior
to race

Reference
MacDowall et al

Renzetti and Gobran



Schoettlin and
Landau





Wayne et al.


            ^Calculated from a measured value of 0.25 ppm (phenolphthalein method) which is equivalent to 0.13 ppm by the KI method.

-------
        and 10-3 present these conclusions in
        tabular form.

L.  RESUME'

   Under the conditions prevailing in the areas
where studies were conducted, adverse health
effects, as  shown  by impairment  of perfpr-
mance  of  student athletes, occurred over a
range  of hourly average oxidant  concentra-
tions  from  60 to 590 jug/m3 (0.03  to  0.3
ppm).   An   increased  frequency  of asthma
attacks in a small proportion of subjects with
this disease was shown on days when oxidant
concentrations  exceeded  peak values of 250
jug/m3   (0.13 ppm),  a level  that  would  be
associated with an hourly average concentra-
tion ranging from  100 to 120jug/m3 (0.05 to
0.06 ppm). Adverse  health effects, as mani-
fested  by  eye  irritation, were  reported  by
subjects in  several studies when photochemi-
cal oxidant  concentrations  reached  instan-
taneous  levels  of  about 200  pg/m3  (0.10
ppm), a level that would be associated with an
hourly average concentration ranging from 60
to 100 jug/m3 (0.03 to 0.05 ppm).
   Adverse effects on sensitive vegetation were
observed from exposure to photochemical
oxidant concentrations  of about  100 /ug/m3
(0.05 ppm) for 4 hours. Adverse effects  on
materials from exposure to photochemical
oxidants have not been precisely quantified,
but have been observed at the levels presently
occurring in many urban atmospheres.
   It is  reasonable and  prudent to conclude
that, when  promulgating ambient air quality
standards, consideration  should be  given  to
requirements for margins of safety that would
take into account  possible effects on health,
vegetation,  and  materials that might  occur
below the lowest of the above levels.
                                                                                  10-13

-------
                                                                 AP-63
                                 ERRATA FOR



               AIR QUALITY CRITERIA FOR PHOTOCHEMICAL OXIDANTS

                            (Summary and Conclusions)
Page 10-7, col. 2, section I, par. 2, lines 7-11:  change to read:  "Peak
     oxidant values ot 4yu ug/m^ (u.tb ppmj, wnich might be expected in
     relation to a maximum hourly average level as low as 300 ug/m3 (0.15 ppm)
     have been associated with aggravation of asthma."

Page 10-8, section I, col. 1, par. 2, lines 3 and 4:  change "ranged from
     60 to 590 ug/m3 (0.03 ppm to 0.3 ppm)" to read "exceeded 130 ug/m3
     (0.07 ppm)"

Page 10-8f section If col. 1. par. 2. lines 9-13:  delete sentence "This
     oxidant value...localized conditions."

Page 10-10f col. lf section l.b.fl). lines 2 and 3:  change "250 ug/m3
     (0.13 ppm)" to read "490 ug/rn^ (0.25 ppm)"

Page 10-10. col. 1. section l.b.(l), lines 9 and 10:  change "of 100 to
     120 ug/m3 (0.05 to 0.06 ppm)" to read "as low as 300 ug/m3 (0.15 ppm)"

Page 10-10, col. 1 and 2, section l.b.(2) (a), lines 4-7:  delete sentence
     beginning "Sucli a peak..."                          "

Page 10-10. col. 2, section l.b.(2)(a), lines 1 and 2:  add "(Chapter 9,
     section B.5.)" to end of previous sentence ( in column 1).

Page 10-10. col. 2, section l.b.(2)(b), lines 3 and 4:  change "ranging
     from 60 to 590 ug/m3 (0.03 to 0.30 ppm)" to read "in excess of 130
     ug/m3 (0.07 ppm)"

Page 10-12, Table 10-3, column 5, third comment:  delete comment "Such a
     peak value...(0.025 to 0.05 ppm)."

Page 10-12, Table 10-3, column 2, entry 5:  change "0.13a" to read "0.25"

Page 10-12, Table 10-3, column 3, entry 3:  change "250" to "490"
                                                               (OVER)

-------
 Page 10-12, Table 10-5, column 5, fifth comment, lines 3 and 4:   change
      "of 100 to 120 ug/m3 (0.05 to 0.06 ppm)" to read "as low as 300 ug/m3
      (0.15 ppm)"

 Page 10-12  Table 10-3, columns 2 and 3, fourth entry:  Add the  word
     "Exceeding" (as above Tor eye irritation)

 Page 10-12, Table 10-3, column 2, fourth entry:   change "0.03 to 0.30" to
      "0.07"

 Page 10-12, Table 10-5. column 3. fourth entry:   change "60 to 590" to "130"

 Page 10-12, Table 10-3, footnote:  delete footnote.

 Page 10-13, col.  1,  section  L, par. 1.  lines  4-6:   change "over  a range of
      hourly average oxidant  concentrations from 60 to 590 ug/m3  (0.03 to
      0.3 ppm)"  to read "when the hourly average oxidant concentrations
      exceeded 130 ug/m3 (0.07 ppm)"

 Page 10-13,  col.  1,  section  L, par. 1,  lines  10  and 11:   change  "250 ug/m3
      (0.13  ppm)"to "490 ug/m-5 (0,25 ppm)"

 Page 10-15,  col.  I,  sectign  L, par. 1,  lines  13  and 14:   change  "ranging
      from 100 to  120 ug/m5 (0.05 to 0.06 ppm)  to read "as low as 300 ug/m3
      (0.15  ppm)."

 Page 10-15,  section  L,  col.  2, par. 1,  lines  3-5:  delete "a level  that...
      (0.03  to 0.05 ppm)".
JCR/ps/9-17-70

-------